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Causes and Effects of Cerebral Ischemia - Oren Zarif - Cerebral Ischemia


There are several causes of cerebral ischemia, including heart attacks. Generally, the cause of ischemia is extremely low blood pressure, which leads to the tissue not receiving enough oxygen. Heart attacks slow down the blood flow, causing blood clots and eventually stopping blood flow to the major organs. Other causes of cerebral ischemia include a congenital heart defect and other illnesses. In such cases, cerebral ischemia is a complication of the heart disease.

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Cerebral ischemia reduces the supply of glucose and oxygen to brain tissue, leading to brain injury and gliosis. Global cerebral ischemia may occur due to cardiac arrest, carotid occlusion, or hypotension, while focal cerebral ischemia is often caused by vascular atherosclerosis. In both types of cerebral ischemia, abnormally high calcium ions enter the neurons, causing cell death. The high calcium levels activate endonucleases and proteases, causing structural protein and DNA damage.

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Initial workup for cerebral ischemia involves a cranial CT scan and a physical exam. A comprehensive blood count and coagulation factors should be performed to rule out other possible causes of stroke. EKG and cardiac enzymes should also be performed. A stat non-contrast head CT will also be necessary to rule out a mass lesion or hemorrhage. Vascular imaging may be useful for distinguishing ischemic stroke from other causes of brain tissue death.

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Among the various causes of cerebral ischemia, ventricular fibrillation mimics clinical cardiac arrest. To study the effects of ventricular fibrillation, researchers have added cardiopulmonary resuscitation to cardiac arrest. The use of cardiopulmonary resuscitation during ventricular fibrillation is usually successful. The use of epinephrine and chest compressions can restore cerebral blood flow. Acute cerebral ischemia can be a life-threatening emergency.

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Ischemic stroke typically presents with rapid onset neurological deficit. Symptoms may improve or worsen depending on the fate of the ischemic penumbra. Ischemia is a medical emergency, which can lead to global hypoxic-ischemic encephalopathy. The effects of cerebral ischemia can be devastating, and treatment for ischemic stroke is critical. In this activity, we examine the causes, highlights the importance of an interprofessional team in evaluation, and summarize the management options for cerebral ischemia.

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Neurocritical care specialists are the best people to consult when considering treatment options for this potentially life-threatening condition. These specialists include Dreier MN, Bleck TP, Major S, Manning AI, Shutter L, Vespa P, Bruder N, Maurer L, Lanzino G, Rabinstein A, and Schmutzhard E. Neurocritical care specialists should be consulted immediately if a patient experiences cerebral ischemia.

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After ischemic brain injury, animals are in a comatose state for 24 hours. This coma can be reversed and normal neurological function can resume. Studies by Kabat et al. and Grenell showed that the ischemic state results in significant brain damage. However, this is still a very basic model and requires further research and validation. If you are looking for a more accurate way to assess the risk of cerebral ischemia in patients, consider a 3-VO model.

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In addition to a standardized stroke assessment, doctors should consider the underlying cause of the condition. Some causes of cerebral ischemia are cardioembolic and embolic. The causes of these conditions vary widely, but they all result in a reduction in the overall blood flow to the brain. Patients with a history of ischemia are more likely to develop it than people without it. Moreover, men are more likely to develop ischemia than women and are more likely to experience strokes than women.

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The goal of identifying ischemic stroke is to determine the CBF, which is the amount of blood flowing through the brain. The normal range of cerebral blood flow is 50 mL/100 g/min (CBF). A CBF lower than that indicates ischemia, which is accompanied by rapid neuronal death. Patients suffering from focal cerebral ischemia have a focal area of severe ischemia and a surrounding region of moderate or mild ischemia. In either case, brain damage occurs and a person becomes unconscious.

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Neuronal necrosis is an early feature of ischemic stroke. Delayed neuronal death occurs months or even years after the initial stroke, although apoptosis may contribute to delayed death. During the early stages of cerebral ischemia, the periinfarct zone comprises up to half of the lesion volume. This area represents an opportunity for neuroprotective poststroke therapy, and recent studies have shown that these neurons are recovering for several days or even weeks.

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Moreover, there is a significant association between BP and adverse outcomes. The association between BP and downstream ischemia was investigated in a large epidemiologic study of pulse pressure in hemodialysis patients. Compared to hypoxic ischemia, ischemic stroke is associated with decreased executive cognitive function. If this relationship between BP and downstream ischemia is established, it will become more pronounced. With a lower limit of cerebral autoregulation, it only makes sense to increase SBP if the underlying condition is severe.

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